Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008241 | SCV001168007 | likely pathogenic | not provided | 2018-07-06 | criteria provided, single submitter | clinical testing | The c.1304dupA variant in the OPTN gene has not been reported previously as a pathogenic variant nor as a benign variant, to our knowledge. The c.1304dupA variant causes a frameshift starting with codon Alanine 436, changes this amino acid to a Glycine residue, and creates a premature Stop codon at position 11 of the new reading frame, denoted p.Ala436GlyfsX11. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The c.1304dupA variant is not observed in large population cohorts (Lek et al., 2016). |
Labcorp Genetics |
RCV002549284 | SCV003481300 | pathogenic | Primary open angle glaucoma; Amyotrophic lateral sclerosis type 12; Glaucoma 1, open angle, E | 2022-12-20 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 817138). This sequence change creates a premature translational stop signal (p.Ala436Glyfs*11) in the OPTN gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in OPTN are known to be pathogenic (PMID: 20428114). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with OPTN-related conditions. |